ArticleNature communications2025
Dendritic cell progenitors engineered to express extracellular-vesicle-internalizing receptors enhance cancer immunotherapy in mouse models.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Insights into extracellular vesicles: From biogenesis and tumor immune modulation to their clinical potential in immunotherapy.Molecular therapy. Nucleic acids · 2026Review
- Dendritic cell diversity and dysfunction in cancer: implications for immunotherapy and therapeutic targeting.Acta pharmacologica Sinica · 2026Review
- Beyond CAR-T and oncology: broadening chimeric antigen receptor technologies across cell types and diseases.Precision clinical medicine · 2026Review
- CAR-T cell therapies are coming after glioblastoma: An overview of early phase clinical trials and future perspectives.iScience · 2026Review
- Roles and potential applications of non-coding RNAs in cancer treatment with immune checkpoint inhibitors and immunomodulatory therapies.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Precision Engineering of Extracellular Vesicles as Programmable Carriers for mRNA Therapeutics.International journal of nanomedicine · 2026Review
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.Frontiers in immunology · 2026Review
- Rearming mesenchymal stem cells with engineering strategies to combat cancer.Frontiers in immunology · 2026Review
- Dendritic Cell Therapy in Immuno-Oncology: A Potentially Key Component of Anti-Cancer Immunotherapies.Cancers · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Cancer immunotherapy using dendritic cells (DC) pulsed ex vivo with tumour antigens is considered safe, but its clinical efficacy is generally modest. Here we engineer DC progenitors (DCP), which can replenish conventional type 1 DCs (cDC1) in mice, to constitutively express IL-12 together with a non-signalling chimeric receptor, termed extracellular vesicle-internalizing receptor (EVIR). By binding to a bait molecule (GD2 disialoganglioside) expressed on cancer cells and their EVs, the EVIR enforces EV internalization by cDC1 to promote their cross-dressing with preformed, tumour-derived MHCI-peptide complexes. Upon systemic deployment to mice, the engineered DCPs cause only mild and transient elevation of liver enzymes, acquire tumour-derived material, engage tumour-specific T cells, and enhance the efficacy of PD-1 blockade in an immunotherapy-resistant melanoma model comprising both GD2-positive and -negative cancer cells, without the need for ex vivo antigen pulsing. These results indicate that EVIR-engineered DCPs may avert the positive selection of antigen-negative cancer cells, potentially addressing a critical limitation of immunotherapies targeting defined tumour antigens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.